ubiquinone and 2-n-butylmalonate

In isolated potato tuber mitochondria, palmitic acid (PA) can induce a H+ leak inhibited by GTP in the phosphorylating (state 3) respiration but not in the resting (state 4) respiration. The PA-induced H+ leak is constant when state 3 respiration is decreased by an inhibition of the succinate uptake with n-butyl malonate (nBM). We show that the efficiency of inhibition by GTP is decreased when state 3 respiration is progressively inhibited by antimycin A (AA) and is restored following subsequent addition of nBM. We propose that in phosphorylating potato tuber mitochondria, the redox state of ubiquinone, which can antagonistically be varied with AA and nBM, modulates inhibition of the PA-activated UCP-sustained H+ leak by GTP.

Topics: Cell Respiration; Dactinomycin; Electrons; Fatty Acids, Nonesterified; Guanosine Triphosphate; Intracellular Membranes; Malonates; Membrane Proteins; Mitochondria; Mitochondrial Proteins; Oxidation-Reduction; Oxidative Phosphorylation; Palmitic Acid; Plant Proteins; Plant Tubers; Protons; Solanum tuberosum; Ubiquinone